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[PMID]:27036372
[Au] Autor:Rysnik O; McHugh K; van Duivenvoorde L; van Tok M; Guggino G; Taurog J; Kollnberger S; Ciccia F; Baeten D; Bowness P
[Ad] Endereço:Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Science, University of Oxford, Oxford, UK. Electronic address: oliwia.rysnik@gtc.ox.ac.uk.
[Ti] Título:Non-conventional forms of HLA-B27 are expressed in spondyloarthritis joints and gut tissue.
[So] Source:J Autoimmun;70:12-21, 2016 06.
[Is] ISSN:1095-9157
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Human leukocyte antigen (HLA)-B27 (B27) is the strongest genetic factor associated with development of Ankylosing Spondylitis and other spondyloarthropathies (SpA), yet the role it plays in disease pathogenesis remains unclear. We investigated the expression of potentially pathogenic non-conventional heavy chain forms (NC) of B27 in synovial and intestinal tissues obtained from SpA patients. We also determined the presence of NC-B27 in joints, lymphoid and gastrointestinal tissue from B27 transgenic (TG(1)) rats with M.tuberculosis-induced SpA. METHODS: Expression of NC-B27 in human SpA joints and gut and in (21-3 × 283-2)F1 HLA-B27/Huß2m rat tissue was determined by immunohistochemistry, flow cytometry and confocal microscopy analysis using HC10 and HD6 antibodies. RESULTS: Both HC10- and HD6-reactive HLA molecules were present in synovial tissue from SpA patients. Both NC-B27 and KIR3DL2, a ligand for NC-B27, were expressed in inflamed terminal ileal tissues in patients with early SpA. Infiltrating cells in inflamed joint tissues isolated from B27 TG(1) rats expressed high levels of NC-B27. NC-B27 were also expressed in joint-resident cells from ankle and tail joints of B27 TG(1) rats prior to clinical arthritis. The expression of NC-B27 on B27 TG(1) rat CD11b/c(+), CD8α(+), cells from spleens and LNs increased with animal age and disease progression. CONCLUSIONS: Non-conventional HLA class 1 molecules are expressed on resident and infiltrating cells in both synovial and GI tissues in human SpA. NC-B27 expression in joints and lymphoid tissues from B27 TG(1) rats prior to the onset of arthritis is consistent with the hypothesis that they play a pathogenic role in SpA.
[Mh] Termos MeSH primário: Gastroenteropatias/genética
Expressão Gênica
Antígeno HLA-B27/genética
Espondilite Anquilosante/genética
[Mh] Termos MeSH secundário: Animais
Artrite Experimental
Remodelação Óssea/genética
Remodelação Óssea/imunologia
Antígenos CD11/metabolismo
Antígenos CD8/metabolismo
Modelos Animais de Doenças
Gastroenteropatias/imunologia
Gastroenteropatias/metabolismo
Gastroenteropatias/patologia
Antígeno HLA-B27/imunologia
Antígeno HLA-B27/metabolismo
Antígenos de Histocompatibilidade Classe I/genética
Antígenos de Histocompatibilidade Classe I/imunologia
Antígenos de Histocompatibilidade Classe I/metabolismo
Seres Humanos
Ratos
Ratos Transgênicos
Receptores KIR3DL2/genética
Receptores KIR3DL2/metabolismo
Espondilite Anquilosante/imunologia
Espondilite Anquilosante/metabolismo
Espondilite Anquilosante/patologia
Membrana Sinovial/metabolismo
Membrana Sinovial/patologia
alfa-Defensinas/genética
alfa-Defensinas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CD11 Antigens); 0 (CD8 Antigens); 0 (CD8 antigen, alpha chain); 0 (HLA-B27 Antigen); 0 (Histocompatibility Antigens Class I); 0 (Receptors, KIR3DL2); 0 (alpha-Defensins); 0 (alpha-defensin 6, human)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160403
[St] Status:MEDLINE


  2 / 97 MEDLINE  
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[PMID]:26928464
[Au] Autor:Song S; Miranda CJ; Braun L; Meyer K; Frakes AE; Ferraiuolo L; Likhite S; Bevan AK; Foust KD; McConnell MJ; Walker CM; Kaspar BK
[Ad] Endereço:Center for Gene Therapy, The Research Institute at Nationwide Children's Hospital, Columbus, Ohio, USA.
[Ti] Título:Major histocompatibility complex class I molecules protect motor neurons from astrocyte-induced toxicity in amyotrophic lateral sclerosis.
[So] Source:Nat Med;22(4):397-403, 2016 Apr.
[Is] ISSN:1546-170X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Astrocytes isolated from individuals with amyotrophic lateral sclerosis (ALS) are toxic to motor neurons (MNs) and play a non-cell autonomous role in disease pathogenesis. The mechanisms underlying the susceptibility of MNs to cell death remain unclear. Here we report that astrocytes derived from either mice bearing mutations in genes associated with ALS or human subjects with ALS reduce the expression of major histocompatibility complex class I (MHCI) molecules on MNs; reduced MHCI expression makes these MNs susceptible to astrocyte-induced cell death. Increasing MHCI expression on MNs increases survival and motor performance in a mouse model of ALS and protects MNs against astrocyte toxicity. Overexpression of a single MHCI molecule, HLA-F, protects human MNs from ALS astrocyte-mediated toxicity, whereas knockdown of its receptor, the killer cell immunoglobulin-like receptor KIR3DL2, on human astrocytes results in enhanced MN death. Thus, our data indicate that, in ALS, loss of MHCI expression on MNs renders them more vulnerable to astrocyte-mediated toxicity.
[Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/genética
Antígenos de Histocompatibilidade Classe I/biossíntese
Neurônios Motores/patologia
Receptores KIR3DL2/genética
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Esclerose Amiotrófica Lateral/patologia
Animais
Astrócitos/metabolismo
Astrócitos/patologia
Cadáver
Morte Celular/genética
Modelos Animais de Doenças
Feminino
Regulação da Expressão Gênica
Antígenos de Histocompatibilidade Classe I/genética
Seres Humanos
Masculino
Camundongos
Camundongos Transgênicos
Meia-Idade
Mutação
Superóxido Dismutase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HLA-F antigens); 0 (Histocompatibility Antigens Class I); 0 (KIR3DL2 protein, human); 0 (Receptors, KIR3DL2); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:170718
[Lr] Data última revisão:
170718
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160302
[St] Status:MEDLINE
[do] DOI:10.1038/nm.4052


  3 / 97 MEDLINE  
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[PMID]:26888639
[Au] Autor:Zwolinska K; Blachowicz O; Tomczyk T; Knysz B; Gasiorowski J; Zalewska M; Orzechowska BU; Sochocka M; Piasecki E
[Ad] Endereço:Laboratory of Virology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Weigla 12, 53-114, Wroclaw, Poland. kjzwolinska@iitd.pan.wroc.pl.
[Ti] Título:The effects of killer cell immunoglobulin-like receptor (KIR) genes on susceptibility to HIV-1 infection in the Polish population.
[So] Source:Immunogenetics;68(5):327-37, 2016 May.
[Is] ISSN:1432-1211
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Killer cell immunoglobulin-like receptors (KIR) are the most polymorphic receptors of natural killer (NK) cells. Their activity diversifies the functions of NK cells in the antiviral immune response, so the presence of certain KIR may affect transmission of HIV-1. The aim of the study was to evaluate the influence of KIR genes on the susceptibility to HIV-1 infection in the Polish population depending on the route of exposure. We determined the frequencies of activating (2DS1, 2DS2, 2DS3, 2DS4f, 2DS4del, 2DS5, 3DS1) and inhibitory (2DL1, 2DL2, 2DL3, 2DL5, 3DL1) KIRs in HIV-1-positive patients (n = 459), individuals exposed to HIV-1 but uninfected (EU, n = 118) and in uninfected, healthy blood donors (BD, n = 98). Analysis was performed using stepwise logistic regression. Apart from KIRs, CCR5-∆32, and CCR2-64I, alleles were also analyzed, as we knew or suspected that these features could affect susceptibility to HIV infection. The regression confirmed the protective effect of CCR5-∆32 (OR = 0.25, p = 0.006) and CCR2-64I (OR = 0.59, p = 0.032) against HIV infection. Among KIR genes, 2DL3 was found to be a protective factor (OR = 0.30, p = 0.015). A similar effect was seen for 3DS1 but only in intravenous drug users (IDUs) (OR = 0.30, p = 0.019), not in sexually exposed people. 2DL5 was found to be a factor facilitating HIV infection (OR = 2.13, p = 0.013). A similar effect was observed for 2DL2 but only in females (OR = 2.15, p = 0.040), and 2DS1 in IDUs (OR = 3.03, p = 0.022). Our results suggest a beneficial role of KIR3DS1 and 2DL3 supporting resistance to HIV infection and a harmful effect of 2DS1, 2DL5, and 2DL2 genes promoting HIV acquisition.
[Mh] Termos MeSH primário: Suscetibilidade a Doenças
Infecções por HIV/genética
HIV-1/genética
Polimorfismo Genético/genética
Receptores KIR/genética
[Mh] Termos MeSH secundário: Adulto
Estudos de Casos e Controles
Feminino
Frequência do Gene
Genótipo
Infecções por HIV/epidemiologia
Infecções por HIV/virologia
Seres Humanos
Células Matadoras Naturais/metabolismo
Masculino
Polônia/epidemiologia
Receptores KIR3DL1/genética
Receptores KIR3DL2/genética
Receptores KIR3DS1/genética
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, KIR); 0 (Receptors, KIR3DL1); 0 (Receptors, KIR3DL2); 0 (Receptors, KIR3DS1)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160219
[St] Status:MEDLINE
[do] DOI:10.1007/s00251-016-0906-1


  4 / 97 MEDLINE  
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[PMID]:26841353
[Au] Autor:Ridley A; Hatano H; Wong-Baeza I; Shaw J; Matthews KK; Al-Mossawi H; Ladell K; Price DA; Bowness P; Kollnberger S
[Ad] Endereço:Botnar Research Centre, Nuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Oxford University, Oxford, UK.
[Ti] Título:Activation-Induced Killer Cell Immunoglobulin-like Receptor 3DL2 Binding to HLA-B27 Licenses Pathogenic T Cell Differentiation in Spondyloarthritis.
[So] Source:Arthritis Rheumatol;68(4):901-14, 2016 Apr.
[Is] ISSN:2326-5205
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: In the spondyloarthritides (SpA), increased numbers of CD4+ T cells express killer cell immunoglobulin-like receptor 3DL2 (KIR-3DL2). The aim of this study was to determine the factors that induce KIR-3DL2 expression, and to characterize the relationship between HLA-B27 and the phenotype and function of KIR-3DL2-expressing CD4+ T cells in SpA. METHODS: In total, 34 B27+ patients with SpA, 28 age- and sex-matched healthy controls (20 B27- and 8 B27+), and 9 patients with rheumatoid arthritis were studied. KIR-3DL2 expression and other phenotypic characteristics of peripheral blood and synovial fluid CD4+ T cells were studied by flow cytometry, quantitative polymerase chain reaction, and Western blotting. T cell receptor clonality was determined by template-switch anchored reverse transcription-polymerase chain reaction and sequencing analysis. Cytokines were measured by enzyme-linked immunosorbent assay. RESULTS: Cellular activation induced KIR-3DL2 expression on both naive and effector CD4+ T cells. KIR-3DL2 binding to B27+ cells promoted expression of KIR-3DL2, the Th17-specific transcription factor retinoic acid receptor-related orphan nuclear receptor γt, and the antiapoptotic factor B cell lymphoma 2. KIR-3DL2+CD4+ T cells in patients with ankylosing spondylitis were oligoclonal and enriched for markers of T cell activation and for the gut homing receptor CCR9. In the presence of B27+ antigen-presenting cells, KIR-3DL2+CD4+ T cells produced less interleukin-2 (IL-2) but more IL-17. This effect was blocked by HC10, an antibody that inhibits the binding of KIR-3DL2 to B27 heavy chains. CONCLUSION: KIR-3DL2 binding to HLA-B27 licenses Th17 cell differentiation in SpA. These findings raise the therapeutic potential of targeting HLA-B27-KIR-3DL2 interactions for the treatment of B27+ patients with SpA.
[Mh] Termos MeSH primário: Diferenciação Celular/imunologia
Antígeno HLA-B27/imunologia
Receptores KIR3DL2/imunologia
Espondiloartropatias/imunologia
Células Th17/imunologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Artrite Psoriásica/imunologia
Artrite Reativa/imunologia
Artrite Reumatoide/imunologia
Western Blotting
Linfócitos T CD4-Positivos/imunologia
Estudos de Casos e Controles
Citocinas/imunologia
Ensaio de Imunoadsorção Enzimática
Feminino
Citometria de Fluxo
Antígeno HLA-B27/metabolismo
Seres Humanos
Masculino
Meia-Idade
Receptores de Antígenos de Linfócitos T/genética
Receptores KIR3DL2/metabolismo
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Espondilite Anquilosante/imunologia
Linfócitos T/imunologia
Transcriptoma
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (HLA-B27 Antigen); 0 (KIR3DL2 protein, human); 0 (Receptors, Antigen, T-Cell); 0 (Receptors, KIR3DL2)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160204
[St] Status:MEDLINE
[do] DOI:10.1002/art.39515


  5 / 97 MEDLINE  
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[PMID]:26260270
[Au] Autor:Abi-Rached L; Guethlein LA; Norman PJ; Parham P
[Ad] Endereço:Departments of Structural Biology and Microbiology and Immunology, Stanford University, Fairchild D-159, 299 Campus Drive West, Stanford, CA, 94305, USA.
[Ti] Título:Chimpanzee susceptibility to hepatitis C virus infection correlates with presence of Pt-KIR3DS2 and Pt-KIR2DL9: paired activating and inhibitory natural killer cell receptors.
[So] Source:Immunogenetics;67(10):625-8, 2015 Oct.
[Is] ISSN:1432-1211
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Infection of humans and chimpanzees with Hepatitis C virus (HCV) results in either the resolution of the acute infection or its progression to a persistent infection associated with chronic liver disease. In cohorts of human patients, resolution of HCV infection has been associated with homozygosity for both C1(+)HLA-C and its cognate inhibitory receptor, KIR2DL3. Compared here are the killer cell immunoglobulin-like receptors (KIR) and major histocompatibility complex (MHC) class I factors of chimpanzees who resolve, or resist, HCV infection with those chimpanzees who progress to chronic infection. Analysis of Pt-KIR gene content diversity associated two of the 12 Pt-KIR with clinical outcome. Activating Pt-KIR3DS2 and inhibitory Pt-KIR2DL9 are strong receptors specific for the C2 epitope. They are encoded by neighboring genes within the Pt-KIR locus that are in strong linkage disequilibrium. HCV-infected chimpanzees with KIR genotypes containing Pt-KIR3DS2 and KIR2DL9 are significantly more likely to progress to chronic infection than infected chimpanzees lacking the genes (p = 0.0123 and p = 0.0045, respectively), whereas human HLA-B allotypes having the C1 epitope are unusual, such allotypes comprise about one quarter of the chimpanzee Patr-B allotypes. Homozygous C1 (+) Patr-B are enriched in chimpanzees with chronic HCV infection, and the compound genotype of homozygous C1 (+) Patr-B combined with either Pt-KIR3DS2 or Pt-KIR2DL9 is more strongly associated with disease progression than either factor alone (p = 0.0031 and p = 0.0013, respectively). Thus, despite similarities suggesting a common basis in disease resistance, there are substantial differences in the KIR and MHC class I correlations observed for HCV-infected humans and chimpanzees, consistent with the divergence of their KIR and MHC class I systems.
[Mh] Termos MeSH primário: Predisposição Genética para Doença/genética
Hepatite C/genética
Antígenos de Histocompatibilidade Classe I/genética
Pan troglodytes/genética
Receptores KIR/genética
[Mh] Termos MeSH secundário: Animais
Progressão da Doença
Frequência do Gene
Variação Genética
Genótipo
Haplótipos
Hepacivirus/fisiologia
Hepatite C/virologia
Pan troglodytes/virologia
Receptores KIR3DL2/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Histocompatibility Antigens Class I); 0 (Receptors, KIR); 0 (Receptors, KIR3DL2)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150812
[St] Status:MEDLINE
[do] DOI:10.1007/s00251-015-0863-0


  6 / 97 MEDLINE  
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[PMID]:26244610
[Au] Autor:Gaur P; Misra R; Aggarwal A
[Ad] Endereço:Department of Clinical Immunology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, India.
[Ti] Título:Natural killer cell and gamma delta T cell alterations in enthesitis related arthritis category of juvenile idiopathic arthritis.
[So] Source:Clin Immunol;161(2):163-9, 2015 Dec.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Enthesitis related arthritis (ERA) is associated with increased frequency of Th17 cells and synovial fluid (SF) IL-17 levels. Natural killer (NK) and gamma delta T cells have been recently shown to produce IL-17, thus we studied the NK and gamma delta-T cells in peripheral blood (PB) of 50 ERA, 16 other JIA patients and 19 healthy controls. We have analyzed the frequency of NK (total, CD56dim, CD56bright) and gamma delta-T cells, perforin and KIR3DL1/2 expression on NK cells and IL-17 and IFN-gamma production by them using flow cytometry. ERA patients had more NK cells with reduced perforin expression and IFN-gamma production but increased KIR3DL1/2 expression and IL-17 production as compared to controls. Also IL-17 producing gamma delta-T were increased in PB of ERA patients. Paired SF samples had NK cells with reduced perforin and KIR3DL expression. Thus increased NK and gamma delta-T cells may contribute to the inflammation in ERA by producing IL-17.
[Mh] Termos MeSH primário: Artrite Juvenil/imunologia
Células Matadoras Naturais/imunologia
Linfócitos T/imunologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Estudos de Casos e Controles
Criança
Feminino
Seres Humanos
Interferon gama/imunologia
Interleucina-17/imunologia
Masculino
Perforina/imunologia
Receptores KIR3DL1/imunologia
Receptores KIR3DL2/imunologia
Líquido Sinovial/imunologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (IL17A protein, human); 0 (Interleukin-17); 0 (KIR3DL1 protein, human); 0 (KIR3DL2 protein, human); 0 (Receptors, KIR3DL1); 0 (Receptors, KIR3DL2); 126465-35-8 (Perforin); 82115-62-6 (Interferon-gamma)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:151123
[Lr] Data última revisão:
151123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150806
[St] Status:MEDLINE


  7 / 97 MEDLINE  
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[PMID]:25940819
[Au] Autor:Vendelbosch S; de Boer M; van der Heijde D; van den Berg TK; van Gaalen FA; Kuijpers TW
[Ad] Endereço:Department of Blood Cell Research, Sanquin Research and Landsteiner Laboratory, Amsterdam, the Netherlands.
[Ti] Título:KIR3DL1 and KIR3DL2 gene copy number variation in axial spondyloarthritis.
[So] Source:Tissue Antigens;85(6):497-8, 2015 Jun.
[Is] ISSN:1399-0039
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Dosagem de Genes
Receptores KIR3DL1/genética
Receptores KIR3DL2/genética
Espondilartrite/genética
Espondilite Anquilosante/genética
[Mh] Termos MeSH secundário: Adulto
Estudos de Coortes
Feminino
Seres Humanos
Masculino
Países Baixos/epidemiologia
Espondilartrite/epidemiologia
Espondilite Anquilosante/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (KIR3DL1 protein, human); 0 (KIR3DL2 protein, human); 0 (Receptors, KIR3DL1); 0 (Receptors, KIR3DL2)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150505
[Lr] Data última revisão:
150505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150506
[St] Status:MEDLINE
[do] DOI:10.1111/tan.12563


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[PMID]:25867094
[Au] Autor:Augusto DG; O'Connor GM; Lobo-Alves SC; Bass S; Martin MP; Carrington M; McVicar DW; Petzl-Erler ML
[Ad] Endereço:Departamento de Genética, Universidade Federal do Paraná, Curitiba, PR, Brazil.
[Ti] Título:Pemphigus is associated with KIR3DL2 expression levels and provides evidence that KIR3DL2 may bind HLA-A3 and A11 in vivo.
[So] Source:Eur J Immunol;45(7):2052-60, 2015 Jul.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Although HLA-A3 and A11 have been reported to be ligands for KIR3DL2, evidence for any in vivo relevance of this interaction is still missing. To explore the functional importance of KIR3DL2 allelic variation, we analyzed the autoimmune disease pemphigus foliaceus, previously associated (lower risk) with activating KIR genes. KIR3DL2*001 was increased in patients (odds ratio (OR) = 2.04; p = 0.007). The risk was higher for the presence of both KIR3DL2*001 and HLA-A3 or A11 (OR = 3.76, p = 0.013), providing the first evidence that HLA-A3 and A11 may interact with KIR3DL2 in vivo. The nonsynonymous single nucleotide polymorphism 1190T (rs3745902) was associated with protection (OR = 0.52, p = 0.018). This SNP results in a threonine-to-methionine substitution. Individuals who have methionine in this position exhibit a lower percentage of KIR3DL2-positive natural killer (NK) cells and also lower intensity of KIR3DL2 on expressing natural killer cells; additionally, we show that the expression of KIR3DL2 is independent of other killer cell immunoglobulin-like receptors. Pemphigus foliaceus is a very unique complex disease strongly associated with immune-related genes. It is the only autoimmune disease known to be endemic, showing a strong correlation with environmental factors. Our data demonstrate that this relatively unknown autoimmune disease may facilitate understanding of the molecular mechanisms of KIR3DL2 ligand recognition.
[Mh] Termos MeSH primário: Predisposição Genética para Doença/genética
Antígeno HLA-A11/genética
Antígeno HLA-A11/metabolismo
Antígeno HLA-A3/genética
Pênfigo/genética
Receptores KIR3DL2/genética
[Mh] Termos MeSH secundário: Citometria de Fluxo
Genótipo
Seres Humanos
Polimorfismo de Nucleotídeo Único
Ligação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (HLA-A11 Antigen); 0 (HLA-A3 Antigen); 0 (KIR3DL2 protein, human); 0 (Receptors, KIR3DL2)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:161203
[Lr] Data última revisão:
161203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150414
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201445324


  9 / 97 MEDLINE  
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[PMID]:25797201
[Au] Autor:Meriem B; Jihen S; Houda K; Ghaya C; Manel C; Hedi B; Slama H
[Ad] Endereço:Immunogenetic Applied to Cell Therapy Research Unit, Immunohematology and HLA-typing Department, National Blood Transfusion Center of Tunis, Tunisia. Electronic address: meriem.bani@yahoo.com.
[Ti] Título:Killer cell immunoglobulin-like receptor (KIR) locus profiles in the Tunisian population.
[So] Source:Hum Immunol;76(5):355-61, 2015 May.
[Is] ISSN:1879-1166
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Killer cell immunoglobulin-like receptors (KIRs) are a family of inhibitory and activatory receptors that are expressed by most natural killer (NK) cells. The KIR gene family is polymorphic: genomic diversity is achieved through differences in gene content and allelic polymorphism. The number of KIR loci has been reported to vary among individuals, resulting in different KIR haplotypes. In this study we report the genotypic structure of KIRs in 267 unrelated and healthy Tunisian subjects by polymerase chain reaction-sequence-specific primer (PCR-SSP) method. All 16 KIR genes were observed in the population with different frequencies; framework genes KIR3DP1 and KIR3DL2 and the nonframework genes KIR2DL1 and KIR2DP1 were present in all individuals. A total of 26 different KIR gene profiles and 54 subgenotypes were observed in the tested population samples. Genotype 1, with a frequency of 36.6%, is the most commonly observed in the Tunisian population. Our results showed that the Tunisian population possesses the previously reported general features of the Caucasian as well as African populations, with some additional interesting differences. Such knowledge of the KIR gene distribution in populations is very useful in the study of associations with diseases and in selection of donors for haploidentical bone marrow transplantation.
[Mh] Termos MeSH primário: Grupo com Ancestrais do Continente Africano
Grupo com Ancestrais do Continente Europeu
Células Matadoras Naturais/imunologia
Receptores KIR2DL1/genética
Receptores KIR3DL2/genética
Receptores KIR/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Criança
Pré-Escolar
Feminino
Frequência do Gene
Genótipo
Haplótipos
Seres Humanos
Masculino
Meia-Idade
Polimorfismo Genético
Pseudogenes/genética
Tunísia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (KIR2DL1 protein, human); 0 (KIR3DL2 protein, human); 0 (Receptors, KIR); 0 (Receptors, KIR2DL1); 0 (Receptors, KIR3DL2)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:150502
[Lr] Data última revisão:
150502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150324
[St] Status:MEDLINE


  10 / 97 MEDLINE  
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[PMID]:25582852
[Au] Autor:Hatano H; Shaw J; Marquardt K; Zhang Z; Gauthier L; Chanteux S; Rossi B; Li D; Mitchell J; Kollnberger S
[Ad] Endereço:Botnar Research Centre, Nuffield Department of Rheumatological and Musculoskeletal Sciences, University of Oxford, Oxford OX3 7LD, United Kingdom;
[Ti] Título:The D0 Ig-like domain plays a central role in the stronger binding of KIR3DL2 to B27 free H chain dimers.
[So] Source:J Immunol;194(4):1591-601, 2015 Feb 15.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We proposed that the killer cell Ig-like receptor KIR3DL2 binding more strongly to HLA-B27 (B27) ß2-microglobulin free H chain (FHC) dimers than other HLA-class I molecules regulates lymphocyte function in arthritis and infection. We compared the function of B27 FHC dimers with other class I H chains and identified contact residues in KIR3DL2. B27 FHC dimers interacted functionally with KIR3DL2 on NK and reporter cells more strongly than did other class I FHCs. Mutagenesis identified key residues in the D0 and other Ig-like domains that were shared and distinct from KIR3DL1 for KIR3DL2 binding to B27 and other class I FHCs. We modeled B27 dimer binding to KIR3DL2 and compared experimental mutagenesis data with computational "hot spot" predictions. Modeling predicts that the stronger binding of B27 dimers to KIR3DL2 is mediated by nonsymmetrical complementary contacts of the D0 and D1 domains with the α1, α2, and α3 domains of both B27 H chains. In contrast, the D2 domain primarily contacts residues in the α2 domain of one B27 H chain. These findings provide novel insights about the molecular basis of KIR3DL2 binding to B27 and other ligands and suggest an important role for KIR3DL2-B27 interactions in controlling the function of NK cells in B27(+) individuals.
[Mh] Termos MeSH primário: Antígeno HLA-B27/imunologia
Modelos Moleculares
Multimerização Proteica
Receptores KIR3DL2/metabolismo
[Mh] Termos MeSH secundário: Linhagem Celular
Citometria de Fluxo
Antígeno HLA-B27/química
Seres Humanos
Imunoprecipitação
Células Matadoras Naturais/imunologia
Ligação Proteica/fisiologia
Estrutura Terciária de Proteína/fisiologia
Receptores KIR3DL2/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (HLA-B27 Antigen); 0 (KIR3DL2 protein, human); 0 (Receptors, KIR3DL2)
[Em] Mês de entrada:1504
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150114
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1402214



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